Autologous, third-generation mesothelin-targeted chimeric antigen receptor T cells administered by endoscopic ultrasound–guided intratumoral injection as neoadjuvant therapy for resectable pancreatic ductal adenocarcinoma; the CAR engages mesothelin and signals via CD3ζ with dual co-stimulatory domains to drive cytotoxic killing and cytokine release.
Autologous, third-generation mesothelin-targeted chimeric antigen receptor T cells that bind mesothelin on tumor cells and signal via CD3z with dual co-stimulatory domains to activate T-cell effector functions, leading to proliferation, cytotoxic killing (perforin/granzyme), and cytokine release; delivered by intratumoral endoscopic ultrasound guidance as neoadjuvant therapy for resectable pancreatic ductal adenocarcinoma.
Mesothelin-targeted CAR T cells bind mesothelin on tumor cells and induce T-cell cytotoxicity, primarily via perforin/granzyme-mediated apoptosis (with ancillary Fas–FasL and cytokine effects).
Autologous, genetically engineered chimeric antigen receptor (CAR) T-cell therapy targeting CD19; CAR engagement activates cytotoxic T-cell responses to eliminate CD19+ malignant B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor. After infusion, the CAR binds CD19 on malignant B cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, resulting in targeted elimination of CD19+ B-cell tumors.
CAR-T cells recognize CD19 on target cells and directly kill them via T-cell cytotoxic mechanisms, primarily perforin/granzyme release (and death-receptor signaling).
Intravenous IgG1 monoclonal antibody targeting CD38 on malignant plasma cells; induces ADCC, CDC, ADCP, and direct apoptosis; inhibits CD38 ectoenzyme activity and depletes CD38+ immunosuppressive cells to enhance anti-myeloma immunity.
Isatuximab is an IgG1 monoclonal antibody targeting CD38 on malignant plasma cells. It induces antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP), and can trigger direct apoptosis. It also inhibits CD38 ectoenzyme activity and depletes CD38+ immunosuppressive cells, enhancing anti-myeloma immune responses.
Isatuximab binds CD38 on target cells and mediates Fc-dependent ADCC and ADCP, activates complement (CDC), and can induce direct apoptosis, leading to killing of CD38+ cells.
Autologous T cells genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3ζ signaling domain to activate, expand, and mediate cytotoxic killing of malignant B cells; dual targeting aims to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3zeta signaling domain. Binding to CD19 or CD20 activates and expands the CAR T cells, driving targeted cytotoxic killing of malignant B cells and reducing antigen-loss escape.
CAR T cells recognize CD19 via the CAR and, upon CD3ζ/4-1BB activation, kill target cells through perforin/granzyme-mediated cytolysis and apoptotic pathways.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
Autologous TILs use native TCRs to recognize AFP-derived peptides presented on MHC (primarily class I) on tumor cells, then kill them via cytotoxic T-cell effector mechanisms (perforin/granzyme and Fas–FasL), with supportive cytokines.